Abstract
Chronic heart failure (CHF) is associated with reduced vascular nitric oxide (NO) availability that could affect muscle microvascular O2 pressure (PO2mv) during contractions. We tested the hypothesis that diminished NO availability has a role in the pathological profile of PO2mv in CHF. Spinotrapezius PO2mv was measured (phosphorescence quenching) in female Sprague-Dawley rats 6–10 wk post-myocardial infarction (MI, n = 21; Sham, n = 7) during sodium nitroprusside (SNP, 300 μM), control (CON) and L-nitro arginine methyl ester (L-NAME, 1.5 mM) superfusion. Moderate (n = 15) and Severe (n = 6) CHF were defined based on structural abnormalities (i.e., lung and right-ventricular weights normalized to body weight). Unlike in healthy rats during CON, an undershoot in the PO2mv response, reflecting a dynamic mismatch between O2 delivery (QO2) and uptake (VO2), was seen in CHF rats during SNP (n = 2), CON (n = 12) and L-NAME (n = 19). The results (mean ± SE) for end-contraction PO2mv are shown below. These data demonstrate that despite down-regulation of endothelial NO synthase in CHF, NO still plays an important role in matching O2 delivery to O2 uptake in severe CHF. Supported by AHA (0455582Z)
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